scholarly journals The role of amino acid oxidation in causing ‘specific dynamic action’ in man

1972 ◽  
Vol 27 (1) ◽  
pp. 211-219 ◽  
Author(s):  
J. S. Garrow ◽  
Susan F. Hawes
Keyword(s):  
Amino Acid ◽  
Metabolic Rate ◽  
Resting Metabolic Rate ◽  
Specific Dynamic Action ◽  
Acid Oxidation ◽  
Urea Synthesis ◽  
Dynamic Action ◽  
Urea Production ◽  
Amino Acid Degradation

1. The increase in metabolic rate which occurs after ingestion of protein (the so-called ‘specific dynamic action’) has been attributed to the energy requirements for urea synthesis and amino acid degradation.2. We have tested, in normal adult subjects, the effect of meals which increase or decrease the rate of urea production, and our results do not substantiate this hypothesis.3. The difficulties of accurate measurement of resting metabolic rate are discussed.4. The term ‘specific dynamic action’ is inappropriate since the effect is not specific. We believe that it may prove to be a reflection of protein synthesis rather than of protein catabolism.

Adaptations in protein metabolism during lactation in the rat

1987 ◽  
Vol 58 (3) ◽  
pp. 533-538 ◽  
Author(s):  
Donald J. Naismith ◽  
Siân M. Robinson
Keyword(s):  
Amino Acid ◽  
Protein Metabolism ◽  
Milk Protein ◽  
Acid Oxidation ◽  
Urea Synthesis ◽  
Lean Tissue ◽  
Anabolic Hormone ◽  
Amino Acid Oxidation ◽  
Argininosuccinate Synthase ◽  
Protein Supply

1. The activities of two hepatic enzymes that participate in the regulation of amino acid oxidation and urea synthesis were measured in lactating rats (day 15 of lactation) and virgin controls. The enzymes were alanine aminotransferase (EC 2. 6. 1.2) and argininosuccinate synthase (EC 6. 3. 4.5). Carcasses of the dams were also analysed.2. Changes in the activities of both enzymes in dams fed ad lib. on a diet containing an excess of protein indicated that amino acid oxidation was depressed. In dams restricted in protein to the level of intake of their controls but allowed to satisfy their needs for energy, enzyme activities were significantly reduced. In these animals lean tissue catabolism supplemented the dietary protein supply.3. This adjustment in protein metabolism which effectively spares protein for milk-protein synthesis could be explained either by a reduction in the availability of substrate in the liver, or by the intervention of an anabolic hormone secreted in lactation.

Role of insulin in thermogenic responses to refeeding in 3-day-fasted rats

1983 ◽  
Vol 245 (2) ◽  
pp. E160-E165 ◽  
Author(s):  
N. J. Rothwell ◽  
M. E. Saville ◽  
M. J. Stock
Keyword(s):  
Metabolic Rate ◽  
Resting Metabolic Rate ◽  
Insulin Injection ◽  
Zucker Rats ◽  
Corn Flour ◽  
Plasma Insulin Levels ◽  
Obese Zucker Rats ◽  
Fasted Rats ◽  
Thermogenic Response

Refeeding 3-day-fasted rats with 40 kJ carbohydrate (CHO; corn flour) or protein (gelatin) caused a rise in plasma insulin levels 3 h later, but refeeding fat or injection of norepinephrine (400 micrograms/kg) had no effect. Injection of insulin (0.25 U) caused a 15% rise in metabolic rate 24 h later in fasted rats that could be inhibited by treatment with propranolol. Refeeding rats with a single CHO meal produced an increase in oxygen consumption (15%) 24 h later that was inhibited by injection of diazoxide or 2-deoxy-D-glucose given at the time of the meal. The thermogenic response to insulin injection was unaffected by treatment with diazoxide or 2-deoxy-D-glucose. Genetically obese Zucker rats failed to increase metabolic rate after insulin or CHO. In normally fed lean rats, maintained on a stock diet or a palatable cafeteria diet, insulin (4 U) enhanced the thermogenic response to norepinephrine and stimulated resting metabolic rate (16%) in the cafeteria-fed rats. These data suggest that insulin is involved in the thermogenic responses to food and catecholamines.

PRENATAL NUTRITION OF LAMBS, BEARS—AND BABIES?

PEDIATRICS ◽  
1972 ◽  
Vol 50 (3) ◽  
pp. 357-358
Author(s):  
George F. Cahill
Keyword(s):  
Oxygen Consumption ◽  
Amino Acid ◽  
Calculated Data ◽  
High Rate ◽  
Co2 Production ◽  
Acid Oxidation ◽  
Prenatal Nutrition ◽  
Amino Acid Oxidation ◽  
Urea Production

The two superbly documented papers from the Battaglia group by James et al. and Gresham et al. are most provocative, since they challenge current dogma that glucose is the primary fetal fuel. As evidence, they present several indisputable observations: measured transplacental glucose difference accounts for only 40% of measured fetal oxygen consumption or CO2 production, and a surprisingly high rate of fetal urea production attests to a high rate of amino acid oxidation. The following Table summarizes both their directly determined and their calculated data with several further extrapolations by this reviewer, must have been transferred from mother to fetus.

Roles of urea production, ammonium excretion, and amino acid oxidation in acid-base balance

1986 ◽  
Vol 250 (2) ◽  
pp. F181-F188 ◽  
Author(s):  
W. Mackenzie
Keyword(s):  
Amino Acid ◽  
Acid Oxidation ◽  
Ammonium Excretion ◽  
Acid Base Balance ◽  
Acid Base ◽  
Amino Acid Oxidation ◽  
Titratable Acid ◽  
Urea Production ◽  
Base Balance ◽  
Oxidation Of Methionine

Atkinson and colleagues recently proposed several concepts that contrast with traditional views: first, that acid-base balance is regulated chiefly by the reactions leading to urea production in the liver; second, that ammonium excretion by the kidney plays no role in acid-base homeostasis; and third, that ammonium does not stimulate ureagenesis (except indirectly). To examine these concepts, plasma ions other than bicarbonate are categorized as 1) fixed cations (Na+, K+, Ca2+, and Mg2+, symbolized M+) and anions (Cl-), 2) buffer anions (A-), 3) other anions (X-), and 4) ammonium plus charged amino groups (N+). Since electroneutrality dictates that M+ + N+ = Cl- + HCO3- + A- + X-, it follows that delta HCO3- = delta(M+ - Cl-) - delta A- - delta X- + delta N+. Therefore acid-base disturbances (changes in HCO3-) can be categorized as to how they affect bodily content and hence plasma concentration of each of these four types of ions. The stoichiometry of ureagenesis, glutamine hydrolysis, ammonium and titratable acid excretion, oxidation of neutral, acidic, and basic amino acids, and oxidation of methionine, phosphoserine, and protein are examined to see how they alter these quantities. It is concluded that 1) although ureagenesis is pH dependent and also counteracts a tendency of amino acid oxidation to cause alkalosis, this tendency is inherently limited by the hyperammonemia (delta N+) that necessarily accompanies it, 2) ammonium excretion is equivalent to hydrogen excretion in its effects on acid-base balance if, and only if, it occurs in exchange for sodium or is accompanied by chloride excretion and only when the glutamate generated by glutamine hydrolysis is oxidized.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Ammonia Elevation and Toxicity From Intravenous L-Amino Acid Administration to Dogs: the Protective Role of L-Arginine

1958 ◽  
Vol 192 (2) ◽  
pp. 311-317 ◽  
Author(s):  
John L. Fahey ◽  
Robert S. Perry ◽  
Patricia F. McCoy
Keyword(s):  
Amino Acids ◽  
Amino Acid ◽  
Amino Acid Mixture ◽  
Protective Role ◽  
Ammonium Salts ◽  
Acid Mixture ◽  
Blood Ammonia ◽  
Urea Production ◽  
Acid Administration

A nontoxic intravenous l-amino acid mixture became markedly toxic when l-arginine and l-histidine were deleted from the mixture and was capable of producing convulsions and death in dogs. Associated with these infusions was a marked increase in blood ammonia levels that coincided with the signs of toxicity. Similar toxicity was produced by infusion of ammonium salts. Administration of l-arginine·HCl prior to or with the infused amino acid mixture prevented the toxicity and the blood ammonia rise. Subsequent injection of l-arginine·HCl produced a prompt fall in blood ammonia to normal levels. l-Ornithine·HCl or l-citrulline·HCl were similarly effective. d-Arginine·HCl and l-histidine·HCl were ineffectual. Urea production was more rapid when l-arginine was added to the infused amino acid mixture. The results suggest that the Krebs-Henseleit cycle is a functioning metabolic pathway that normally is a major deterrent to the accumulation of excessive blood ammonia when large amounts of amino acids are infused.

scholarly journals Hepatic detoxification of ammonia in the ovine liver: possible consequences for amino acid catabolism

1995 ◽  
Vol 73 (5) ◽  
pp. 667-685 ◽  
Author(s):  
G. E. Lobley ◽  
A. Connell ◽  
M. A. Lomax ◽  
D. S. Brown ◽  
E. Milne ◽  
...  
Keyword(s):  
Amino Acid ◽  
Kinetic Data ◽  
Free Amino ◽  
Liver Blood Flow ◽  
Whole Body ◽  
Acid Oxidation ◽  
Urea Synthesis ◽  
Amino Acid Oxidation ◽  
N Metabolism ◽  
Glutamate Synthesis

The effects of either low (25 μmol/min) or high (235 μmol/min) infusion of NH4Cl into the mesenteric vein for 5 d were determined on O2consumption plus urea and amino acid transfers across the portal-drained viscera (PDV) and liver of young sheep. Kinetic transfers were followed by use of15NH4Cl for 10 h on the fifth day with simultaneous infusion of [1-13C]lleucine to monitor amino acid oxidation. Neither PDV nor liver blood flow were affected by the additional NH3loading, although at the higher rate there was a trend for increased liver O2consumption. NH3-N extraction by the liver accounted for 64–70% of urea-N synthesis and at the lower infusion rate the additional N required could be more than accounted for by hepatic removal of free amino acids. At the higher rate of NH3administration additional sources of N were apparently required to account fully for urea synthesis. Protein synthesis rates in the PDV and liver were unaffected by NH3infusion but both whole-body (P< 0·05) and splanchnic tissue leucine oxidation were elevated at the higher rate of administration. Substantial synthesis of [15N]glutamine occurred across the liver, particularly with the greater NH3supply, and enrichments exceeded considerably those of glutamate. The [15N]urea synthesized was predominantly as the single labelled, i.e. [14N15N], species. These various kinetic data are compatible with the action of ovine hepatic glutamate dehydrogenase (EC1.4.1.2) in periportal hepatocytes in the direction favouring glutamate deamination. Glutamate synthesis and uptake is probably confined to the perivenous cells which do not synthesize urea. The implications of NH3detoxification to the energy and N metabolism of the ruminant are discussed.

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